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Case Report/Case Series |

Growth Attenuation of Cutaneous Angiosarcoma With Propranolol-Mediated β-Blockade

William Chow, DO1; Clarissa N. Amaya, MS2; Steven Rains, MS2; Michael Chow, BS1; Erin B. Dickerson, PhD3,4; Brad A. Bryan, PhD, MBA2
[+] Author Affiliations
1Mohs Micrographic Surgery and Cutaneous Oncology, San Leandro, California
2Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso
3Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul
4Masonic Cancer Center, University of Minnesota, Minneapolis
JAMA Dermatol. 2015;151(11):1226-1229. doi:10.1001/jamadermatol.2015.2554.
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Importance  Patients with stage T2 multilesion angiosarcomas of the scalp and face that are larger than 10 cm demonstrate a 2-year survival rate of 0%. To our knowledge, major therapeutic advances against this disease have not been reported for decades. Preclinical data indicate that blocking β-adrenergic signaling with propranolol hydrochloride disrupts angiosarcoma cell survival and xenograft angiosarcoma progression.

Observations  A patient presented with a β-adrenergic–positive multifocal stage T2 cutaneous angiosarcoma (≥20 cm) involving 80% of the scalp, left forehead, and left cheek, with no evidence of metastasis. The patient was immediately administered propranolol hydrochloride, 40 mg twice a day, as his workup progressed and treatment options were elucidated. Evaluation of the proliferative index of the tumor before and after only 1 week of propranolol monotherapy revealed a reduction in the proliferative index of the tumor by approximately 34%. A combination of propranolol hydrochloride, 40 mg 3 times a day, paclitaxel, 2 mg/m2 infused weekly, and radiotherapy during the subsequent 8 months resulted in extensive tumor regression with no detectable metastases.

Conclusions and Relevance  Our data suggest that β-blockade alone substantially reduced angiosarcoma proliferation and, in combination with standard therapy, is effective for reducing the size of the tumor and preventing metastases. If successful, β-blockade could be the first major advancement in the treatment of angiosarcoma in decades.

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Figure 1.
Rapid Growth and Extension of the Angiosarcoma Before Treatment

A, Photograph of the patient’s rapidly enlarging tumor in May 2014. B, Hematoxylin-eosin staining confirming the presence of angiosarcoma (original magnification ×400).

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Figure 2.
β-Blockade Reduces the Proliferative Index of the Angiosarcoma

A, Tumor sections were stained for the β-adrenergic receptors ADRB1, ADRB2, and ADRB3. Brown alkaline phosphatase precipitate indicates positive ADRB receptor expression in this angiosarcoma. Negative control staining is depicted in the bottom panels (original magnification ×400). B, Photographs were taken of the patient immediately before propranolol hydrochloride treatment and after 1 week of propranolol monotherapy. C, Ki-67 was detected via immunohistochemistry in the angiosarcoma before treatment and 7 days after propranolol monotherapy. Brown alkaline phosphatase precipitate indicates positive expression for the Ki-67 proliferative marker (original magnification ×400). D, Histogram indicating the mean (SEM) Ki-67 staining in each tumor sample. Ki-67–based proliferative index was quantified via manual counting by an individual (C.N.A.) who was blinded to the tumor data on the same specimen and to the corresponding Ki-67 staining in the sample pair. A fixed number of 800 tumor cells in both the initial and subsequent biopsies were counted from representative areas of the tumor. The asterisk indicates statistical significance as determined by an upaired t test (P < .05).

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Figure 3.
Clear Regression of the Angiosarcoma and Slow, Progressive Healing of the Central Ulceration With No Detectable Metastases

Progressive images of the patient during and following combination therapy with propranolol hydrochloride, paclitaxel, and radiotherapy.

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